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Covalent small ubiquitin-like modifier (SUMO) modification of Maf1 protein controls RNA polymerase III-dependent

Aarti D Rohira1, Chun-Yuan Chen, Justin R Allen

  • 1Department of Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California and the Norris Comprehensive Cancer Center, Los Angeles, California 90033, USA.

The Journal of Biological Chemistry
|May 16, 2013
PubMed

Insights

SUMOylation of Maf1, a transcriptional repressor, is crucial for controlling RNA polymerase III transcription. This modification, regulated by SENP1, impacts gene expression and cell growth, offering new insights into oncogenesis.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Gene Regulation

Background:

  • RNA polymerase III (pol III) transcribes genes vital for cell biosynthesis.
  • Oncogenic transformation involves the induction of these genes.
  • The transcriptional repressor Maf1 is key in repressing oncogenesis-promoting genes.

Purpose of the Study:

  • To investigate the role of SUMOylation in repressing RNA pol III-dependent transcription.
  • To elucidate the mechanism by which SUMOylation affects Maf1 function.
  • To explore the implications of Maf1 SUMOylation in oncogenesis.

Main Methods:

  • Investigated small ubiquitin-like modifier (SUMO) modification of Maf1 by SUMO1 and SUMO2.
  • Identified Lys-35 as the major SUMOylation site on Maf1.
  • Assessed the role of the deSUMOylase SENP1 in controlling Maf1 SUMOylation.
  • Examined the effect of SUMOylation on Maf1's interaction with RNA pol III and its recruitment to promoters.

Main Results:

  • SUMOylation of Maf1 by SUMO1 and SUMO2 was identified as a key mechanism for repressing RNA pol III transcription.
  • Lys-35 was confirmed as the primary SUMOylation site, regulated by SENP1.
  • Maf1 SUMOylation is independent of mTOR signaling.
  • Impaired SUMOylation at Lys-35 hinders Maf1's transcriptional repression and colony growth suppression.
  • SUMOylation does not affect Maf1 localization but impairs its association with RNA pol III, affecting promoter recruitment and dissociation.

Conclusions:

  • SUMOylation of Maf1 is a novel regulatory mechanism controlling RNA pol III transcription.
  • SENP1-mediated deSUMOylation of Maf1 and subsequent gene target induction play a critical role in cancer development.
  • Targeting Maf1 SUMOylation presents a potential therapeutic strategy for cancers driven by aberrant RNA pol III activity.
Keywords:
Post-translational ModificationRNA Polymerase IIITranscription FactorsTranscription RegulationTranscription Repressor

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